Lipids in functional foods in relation to cardiovascular disease

Abstract

Food is considered functional' if it it contains (often added) components that affect one or more targeted functions in the body in a beneficial way. Foods can also be functional if potential harmful components have been removed by technological means. A food can be accepted to be functional only after its potentially beneficial effect has been proven by well-designed and properly executed intervention studies in humans. Cardiovascular disease has a multifactorial etiology, as is illustrated by the existence of numerous risk indicators, many of which can he influenced by diet. It should be recalled, however, that only after a cause-and-effect relationship has been established between the disease and a given risk indicator (called a risk factor in that case), modifying this factor can be expected to affect disease morbidity and mortality, In this presentation, effects of dietary lipids on cardiovascular risk are reviewed, with special emphasis on modification of the plasma lipoprotein profile and of hypertension. In addition, influences of dietary lipids on arterial thrombotic processes and insulin resistance will be discussed. Dietary lipids are able to affect lipoprotein metabolism in a significant way, thereby modifying the risk of cardiovascular disease. However, more research is required concerning the possible interactions between the various dietary fatty acids, and between fatty acids and dietary cholesterol. In addition, more studies are needed with respect to the possible importance of the postprandial state. Certain aspects of blood platelet function, blood coagulability, and fibrinolytic activity are associated with cardiovascular risk, but causality has insufficiently been proven. Nonetheless, well-designed intervention studies should be initiated to further evaluate such promising dietary components as the various n-3 and n-6 fatty acids and their combination for their effect on processes participating in arterial thrombus formation. Although in the etiology of hypertension the genetic component is definitely stronger than environmental factors, some benefit on the development and coronary complications of atherosclerosis in hypertensive patients can be expected from fatty acids such as α-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid. This particularly holds for those subjects where the hypertensive mechanism involves the formation of thromboxane A2 and/or α1-adrenergic activities. However, large-scale trials are required to test this contention. It seems feasible to modulate insulin sensitivity and subsequent cardiovascular risk factors by decreasing the total amount of dietary fat and increasing the proportion of polyunsaturated fatty acids. However, additional studies on the efficacy of specific fatty acids, as well as on the mechanisms involved are required to understand the real function of these dietary components.